Transcript Slide 1

Morphological features of Acute
Viral Hepatitis, Chronic Hepatitis &
Hepatic Fibrosis
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Hepatitis
 Inflammation
of Liver
 Causes: Viral, Alcohol, immune,
Drugs & Toxins
 Types : Acute, Chronic & Fulminant
 Viral Hepatitis :
◦ Specific – Hepatitis A, B, C, D, E
◦ Systemic - CMV, EBV
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Carrier state / Asymptomatic phase
Acute hepatitis
Chronic Hepatitis
◦ Chronic Persistent Hepatitis (CPH)
◦ Chronic Active Hepatitis (CAH)
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Fulminant hepatitis
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Grade1
Grade2
Grade3
Grade 4
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Zonal –
Toxin/Hypoxia
Bridging – Viral severe
Interface – Immune
Apoptotic - Viral
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1 = portal
Stage1
Stage2
3 = septal bridging
Stage3
2 = periportal
4 = bridging with nodular regeneration
Stage4
=cirrhosis
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Swelling , hydropic and ballooning
degeneration , apopptosis
Periportal necrosis
Inflammation – lymphocytes, Macrophages
Mild fatty change – HCV
Portal inflammation and Cholestasis
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Persistent (CPH) & Active (CAH)
Lymphoid aggregates
periportal, piecemeal & bridging necrosis
Periportal, bridging fibrosis
Ground-glass cells (HBV)
Fatty change (HCV)
Apoptosis, lymphocytes & macrophage.
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Areas of necrosis and collapse of liver lobules seen here as illdefined areas that are pale yellow
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-Hepatic failure with in 2-3 weeks.
-Reactivation of chronic or acute
hepatitis
-Massive necrosis, shrinkage, wrinkled
-Little or massive inflammation
-More than a week – regenerative activity
-Complete recovery – or - cirrhosis.
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Grading of
Chronic
Hepatitis
(grade 0-4 )
According to
the degree of
inflammation
and necrosis.
Grade
Portal or pei-portal
Lobular
O
None or mild
none
1
Portal inflammation.
Mild Inflammation.
But no necrosis
2
Mild periportal
inflammation
Focal necrosis
3
Moderate periportal
inflammation.
More necrosis
4
Severe periportal
inflammation.
Severe Necrosis
Staging of
Chronic
Hepatitis
(stage 0-4 )
According
to the
degree of
fibrosis
stage Degree of fibrosis
0
None
1
Minimal portal fibrosis
2
Periportal fibrosis
3
Septal fibrosis with distortion
of architecture.
4
Definite cirrhosis
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Irreversible replacement of normal liver by fibrous connective
tissue
Causes
◦ Chronic inflammation (e.g., chronic hepatitis)
◦ Toxins, usually chronic exposure (e.g., ethanol)
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Sequelae
◦ Altered blood flow & perfusion liver cells
◦ Stages:
 portal (1)
 periportal (2)
 bridging (3)
 cirrhosis (4)
◦ Cirrhosis = diffuse change with nodules of regenerating liver cells
encircled by fibrous scar
Pathogenesis
Fibrosis is not only the result of necrosis, collapse
and scar formation but also the result of
derangements in the synthesis and degradation of
matrix by injured mesenchymal cells that synthesize
the various components of the matrix which in the
liver are the following categories:
1-COLLAGENS
TYPE I,III,V,VI,VII COLLAGEN
2-GLYCOPROTEINS
LAMININ, FIBRONECTIN, ENTACTIN., UNDULIN , ELASTIN&
PROTEOGLYCANS
EVALUATION OF HEPATIC FIBROSIS
HISTOLOGICALLY:
Masson trichrome stain. Siler reticulin stain. Specific antibodies for collagen
types. Dsmin and Vimentin for lipocytes. Vimentin for myofibroblasts.
BIOCHEMICAL:
Determination of various enzymes in matrix synthesis are of very limited
usefulness. Serum laminin in benign fibrosis.
BRIDGING FIBROSIS: Central-central. Connects central veins with
central veins. It is rare and occurring mostly in chronic passive
congestion as in this case.
BRIDGING FIBROSIS: Porto-portal. This form is common
and usually associated with porto-central fibrosis. It follows a
portal inflammation that extends to the terminal,
centroacinar, portal venules.
BRIDGING FIBROSIS: Porto-central. It occurs after centrolobular
necrosis and produces new vascular connections between portal
fields and central veins which may lead to cirrhosis. It is the most
severe form of bridging necrosis and fibrosis and is most of the
times associated with porto-portal fibrosis.
Bridging Fibrosis